an intensive insulin therapy protocol that required glucose determi- nations at least every 2 - 4 hours. Hypoglycemia was defined as 60 mg/dl. Results: Data in the table are shown as means  SEM. Patient Characteristics and Outcomes Day 3 Mean Glucose (mg/dL) N Gender M/F Age (years) BMI Mortality % Sepsis Hypoglycemic Events (60 mg/dL) SICU  150 8 2/6 67  5.3 33.9  5.2 0 0 0 SICU 150 12 6/6 71  2.8 37.2  3.0 7 (58%) 7 (58%) 4 BICU  150 4 1/3 50  12.3 26.4  1.4 0 2 (50%) 2 BICU 150 9 8/1 55  4.4 34.0  3.1 5 (56%) 7 (78%) 1 Admission glucose levels and mean glucose levels for day 1, 2 and 3 for the groups below or equal to 150 mg/dL were 173, 146, 139 and 127 mg/dL in the burn ICU; the corresponding levels in the surgical ICU were 260, 151, 118 and 111 mg/dL. Only the admission levels were significantly different (p0.01). The levels for the groups above 150 mg/dL were 212, 211, 151 and 227 mg/dL in the burn ICU and 205, 165, 158 and 192 mg/dL in the surgical ICU. Percent total burn surface area in the burn ICU patients was 12 and 46 in the 150 and 150 mg/dL groups, respectively. Daily amounts of insulin admin- istered were similar in the two units for all groups. Overall only 36% of surgical ICU/burn ICU patients achieved glycemic goal of 150 mg/dL by day 3 (40% in the surgical ICU and 31% in the burn ICU, pNS), and hypoglycemic events (60 mg/dL) were seen in 20% of patients (none with medical sequellae). Poor glycemic control was exclusively associated with mortality in both burn ICU and surgical ICU patients (57%), and correlated highly with septic events. Con- clusions: Burn mortality is associated with poor glycemic control, percent total body surface area burn, and elevated BMI. We conclude that both surgical ICU and burn ICU patients benefit equally from tight glycemic control obtained by intensive insulin therapy; sepsis- related deaths are reduced by intensive insulin therapy in the burn ICU. QS191. QUANTITATIVE BACTERIOLOGY AND WOUND FAILURE IN HIGH ENERGY PENETRATING WAR INJURIES. Jason Hawksworth 1 , Matthew R. Kasper 2 , Fred Gage 3 , Trevor Brown 3 , Douglas K. Tadaki 3 , Philip Per- due 4 , John Forsberg 7 , Alexander Stojadinovic 8 , Eric A. El- ster 9 ; 1 Department of Surgery, Walter Reed Army Medical Center, Washington D.C., DC; 2 Department of Microbiology, National Naval Medical Center, Bethesda, MD; 3 Regenera- tive Medicine Department, Combat Casualty Care, Naval Medical Research Center, Silver Spring, MD; 4 Department of Surgery, National Naval Medical Center, Bethesda, MD; 7 Department of Orthopedics, National Naval Medical Cen- ter, Bethesda, MD; 8 Department of Surgery, Walter Reed Army Medical Center; Uniformed Services University of Health Sciences; Combat Wound Initiative, Washington D.C., DC; 9 Department of Surgery, National Naval Medical Center; Naval Medical Research Center; Uniformed Ser- vices University of Health Sciences; Combat Wound Initia- tive, Bethesda, MD Introduction: High-energy penetrating war injuries generate complex, contaminated wounds. Patients with these devastating injuries arrive at tertiary care military medical facilities heavily colonized with fastidious environmental bacteria, such as Acineto- bacter baumannii. The cornerstone of war wound management remains surgical debridement to remove devitalized tissue and decrease bacterial colony counts. However, despite aggressive sur- gical management, some wounds fail, often secondary to ongoing infection. Quantitative bacteriology has not previously been stud- ied in acute war wounds and may influence surgical decision making. Methods: Patients with high-energy penetrating extrem- ity wounds sustained during combat in Operation Iraqi Freedom (OIF) were prospectively studied, and followed for 30 days after definitive wound closure. The primary outcome was wound fail- ure, defined as delayed wound closure (21 days from injury) or wound dehiscence. Surgical debridement with VAC application was repeated every 48-72 hours until wound closure. Timing of closure was at the discretion of the attending surgeon. Wound bed tissue biopsy (1 cm 3 ) and VAC effluent (5 mL) were collected prior to each wound debridement and evaluated for quantitative micro- bial counts, reported in colony forming units (CFU) per cm 3 of tissue or effluent. Associations between categorical variables were studied with Fisher’s exact test or Chi-squared test, as appropriate. Results: Nineteen penetrating extremity war wounds (mean size 687 873 cm 3 ) in thirteen male patients (mean age 22 years) were investigated. The mean Injury Severity Score (ISS) was 25 13. There were seven (36.8%) wound failures, including four (21.1%) delayed wound closures and three (15.8%) wound dehiscences. Bacterial colonization (in order of prevalence: Acinetobacter, Staphylococcus Aureus, Enterococcus faecalis, Pseudomonas, and Escherichia coli) was evident in 68.4% and 78.9% of patient wound tissue and effluent, respectively. The presence of associated vascular injury, high ISS (25), and wound colonization correlated with wound failure (p0.05). At time of definitive wound closure, tissue biopsy CFU 10 5 was associated with 67% rate of wound dehiscence (p0.05). Sensitivity, specific- ity, positive and negative predictive value of CFU 10 5 for deter- mining wound failure was 92%, 40%, 81%, 67% respectively. Con- clusions: Tissue quantitative bacteriology is predictive of wound failure in high-energy penetrating war injuries. Additionally, while common in war wounds, microbial colonization in associa- tion with concomitant vascular injury and higher overall injury severity is an important clinical determinant of wound outcome. Given these findings, war wound failure may represent infectious morbidity related to the compensatory counter-inflammatory re- sponse (CARS) to injury. QS192. THE IMPACT OF METHYLATION DEMAND AND HO- MOCYSTEINE METABOLISM ON WOUND GRANU- LATION TISSUE FORMATION. Conrad Hamilton, Kelly Krier, Naveed Saqib, Thomas R. Howdieshell; University of New Mexico HSC, Albuquerque, NM Introduction: Methionine is adenylated to form S-adenosylmethionine, the methyl donor for virtually all known biological methylation reac- tions. The end products of these methyltransferase reactions are a methylated substrate and S-adenosylhomocysteine, which is hydro- lyzed to homocysteine and adenosine. Homocysteine, a known indepen- dent risk factor for atherothrombosis, has not been identified as a risk factor for impaired wound repair. Recent reports suggest that supple- mental arginine may accelerate atherothrombosis via increased homo- cysteine generation. This study was designed to examine the effects of arginine-induced methylation stress and homocysteine generation on wound granulation tissue formation. Methods: A ventral hernia, surgically created in the abdominal wall of 12 swine, was repaired with silicone sheeting and skin closure. An osmotic infusion pump, inserted in a remote subcutaneous pocket, continuously delivered saline solution (n6) or L-Arg (n6) into the wound environment. Granulation tissue thickness was determined by ultrasonography. Fluid was aspirated serially from the developing wound compart- ment for measurement of nitrite/nitrate (NOx), homocysteine, and additional amino acid concentrations. On day 14, the animals were sacrificed, and the abdominal wall was harvested for histo- logic analysis. Data are expressed as mean  SEM. Repeated- 343 ASSOCIATION FOR ACADEMIC SURGERY AND SOCIETY OF UNIVERSITY SURGEONS—ABSTRACTS